Cancer cachexia likely results from a systemic metabolic imbalance where tumors outcompete host tissues for essential nutrients that drive a catabolic process within normal tissues. With an understanding of the metabolic deregulation responsible for cancer cachexia, the condition can be reversed by targeting signaling mechanisms of the tumor and by supplying nutrients to correct metabolic imbalance.

The Ludwig Princeton Branch will explore the biochemical basis by which diet impacts cancer. We will build rational and quantitative understanding of diet’s influence on cancer’s growth, chemotherapy sensitivity, and immune response, and how these factors vary across tumor types and individuals.

One of the hallmarks of cancer is evading an immune response that should recognize emerging cancers as foreign and eliminate them. One way to improve the anti-cancer immune response is by altering metabolism. It is our goal to understand how metabolism in tumor cells, the tumor microenvironment, and immune cells enables immune evasion.

Building on the strength of Princeton in the physical sciences and computation, we will innovate new methods for measuring and manipulating metabolism. The resulting knowledge will be used to develop new treatment regimens that manipulate metabolism to suppress tumor growth and augment antitumor immune response.

Development of successful therapeutic strategies to specifically target metastasis depends on understanding tumor-intrinsic and extrinsic mechanisms that dictate metastatic behaviors. The Ludwig Princeton Branch plays a leading role in the study of cancer metastasis, including signaling networks that regulate cellular plasticity during metastasis, stromal niches that regulate organ-tropic metastasis, metabolic adaptation of metastatic cancer cells, as well as the development of novel anti-metastasis therapeutic agents.